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每一天，你身體內(nèi)的一些細(xì)胞會(huì)停止分裂，這是一件好事。而有些細(xì)胞會(huì)無(wú)限增殖，這是大多數(shù)惡性腫瘤發(fā)展的一個(gè)重要早期步驟。

盡管細(xì)胞無(wú)限增殖在癌癥中有著非常的重要性，但研究人員一直對(duì)于細(xì)胞永生化背后的分子機(jī)制知之甚少。這是因?yàn)榭茖W(xué)家缺乏好方法研究永生化人類細(xì)胞。在發(fā)表在Cell Cycle 雜志上的一項(xiàng)研究中，研究人員已經(jīng)開發(fā)出一種新方法，能夠輕松地創(chuàng)建出不朽的人類乳腺上皮細(xì)胞。

與大多數(shù)人來(lái)源的“不朽”細(xì)胞(包括從腫瘤組織中獲得細(xì)胞)不同，這些新創(chuàng)建的不朽細(xì)胞具有正常的基因組。伯克利實(shí)驗(yàn)室生命科學(xué)部科學(xué)家Martha Stampfer說(shuō)：這些細(xì)胞可能有助于開辟新的策略來(lái)對(duì)抗癌癥。細(xì)胞永生化也可以是一個(gè)重要的治療靶標(biāo)。

Stampfer補(bǔ)充道：現(xiàn)在我們可以獲得攜帶正?；蚪M的無(wú)限增殖的人類乳腺上皮細(xì)胞，去探索細(xì)胞永生化的背后分子機(jī)制，我們也可以開始思考如何針對(duì)細(xì)胞永生化這一過(guò)程，防止或逆轉(zhuǎn)癌癥的發(fā)展。

原文摘要：

Immortalization of normal human mammary epithelial cells in two steps by direct targeting of senescence barriers does not require gross genomic alterations

Hiroyasu Yamamoto, Evan G. Williams, Laurent Mouchiroud, Carles Cantó, Weiwei Fan, Michael Downes, Christophe Héligon, Grant D. Barish, BéatrICE Desvergne, Ronald M. Evans et al.

Telomerase reactivation and immortalization are critical for human carcinoma progression. However, little is known about the mechanisms controlling this crucial step, due in part to the paucity of experimentally tractable model systems that can examine human epithelial cell immortalization as it might occur in vivo. We achieved efficient non-clonal immortalization of normal human mammary epithelial cells (HMEC) by directly targeting the 2 main senescence barriers encountered by cultured HMEC. The stress-associated stasis barrier was bypassed using shRNA to p16INK4; replicative senescence due to critically shortened telomeres was bypassed in post-stasis HMEC by c-MYC transduction. Thus, 2 pathologically relevant oncogenic agents are sufficient to immortally transform normal HMEC. The resultant non-clonal immortalized lines exhibited normal karyotypes. Most human carcinomas contain genomically unstable cells, with widespread instability first observed in vivo in pre-malignant stages; in vitro, instability is seen as finite cells with critically shortened telomeres approach replicative senescence. Our results support our hypotheses that: (1) telomere-dysfunction induced genomic instability in pre-malignant finite cells may generate the errors required for telomerase reactivation and immortalization, as well as many additional “passenger” errors carried forward into resulting carcinomas; (2) genomic instability during cancer progression is needed to generate errors that overcome tumor suppressive barriers, but not required per se; bypassing the senescence barriers by direct targeting eliminated a need for genomic errors to generate immortalization. Achieving efficient HMEC immortalization, in the absence of “passenger” genomic errors, should facilitate examination of telomerase regulation during human carcinoma progression, and exploration of agents that could prevent immortalization.

 干細(xì)胞治療使用的 lonza 12-725F 無(wú)血清培養(yǎng)基 （點(diǎn)擊標(biāo)題進(jìn)入）